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The Chinese Great Famine caused widespread starvation in 1959–1961. Its long-term association with depressive symptoms has not been studied.

Aims

To estimate the burden of depressive symptoms and the association of famine exposure with depressive symptoms.

Method

The China Health and Retirement Longitudinal Study is a nationwide representative survey of 17 708 Chinese adults aged ≥45. Propensity score matching and modified Poisson regression were used to evaluate the association between self-reported famine exposure in early life and depressive symptoms among the overall participants. Such associations were also assessed by developmental stage using modified Poisson regression and logistic regression.

Results

The prevalence of depressive symptoms was 26.2% (95% CI 25.1–27.3%) in 2011. As defined by loss of family members because of starvation, 11.6% (95% CI 10.1–13.1%) of this population experienced severe famine. When compared with participants who did not experience starvation, those who had experienced severe famine during fetal, mid-childhood, young-teenage and early-adulthood stages had 1.87 (95% CI 1.36–2.55), 1.54 (95% CI 1.23–1.94), 1.47 (95% CI 1.09–2.00) and 1.77 (95% CI 1.42–2.21) times higher odds of having depressive symptoms in late adulthood, respectively. The first two trimesters of pregnancy were a critical time window during the fetal stage when severe famine had a stronger association with depressive symptoms. Famine during infant, toddler, preschool or teenage stages was not associated with depressive symptoms. Overall, famine contributed to 13.6% of the depressive symptom burden in this population.

Conclusions

The Chinese Great Famine contributed substantially to the burden of depressive symptoms in China.

Central body fat distribution has been shown to be related to hyperinsulinemia, insulin resistance, hypertriglyceridemia, and atherosclerosis to a greater degree than general obesity. There are known to be both genetic and environmental effects on all components of this clustering. Whether these genetic effects are due to one set of genes in common to the components or whether genetic influences on insulin resistance and/or general/abdominal fatness ‘turn on’ other genes that affect other components of the syndrome is not clear. We analyzed data from the Swedish Adoption/Twin Study of Aging (60% female; monozygotic = 116, dizygotic = 202; average age 65 years) to determine whether there were genetic and/or environmental factors shared among general body fat distribution, abdominal body fat distribution, fasting insulin levels and cardiovascular disease. We found additive genetic effects in males to be significantly different from those in females with genetic effects accounting for variance in waist–hip ratio (males = 28%; females = 49%), body mass index (males = 58%; females = 73%), fasting insulin levels (FI) (males = 27%; females = 49%), and cardiovascular disease (CVD) (males = 18%; females = 37%). There were also shared genetic and environmental effects among all the variables except CVD, but a majority of the genetic variance for these measures was trait specific. Twin Research (2000) 3, 43–50.

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